Go to JCI Insight
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Alerts
  • Advertising
  • Job board
  • Subscribe
  • Contact
  • Current issue
  • Past issues
  • By specialty
    • COVID-19
    • Cardiology
    • Gastroenterology
    • Immunology
    • Metabolism
    • Nephrology
    • Neuroscience
    • Oncology
    • Pulmonology
    • Vascular biology
    • All ...
  • Videos
    • Conversations with Giants in Medicine
    • Author's Takes
  • Reviews
    • View all reviews ...
    • Aging (Upcoming)
    • Next-Generation Sequencing in Medicine (Jun 2022)
    • New Therapeutic Targets in Cardiovascular Diseases (Mar 2022)
    • Immunometabolism (Jan 2022)
    • Circadian Rhythm (Oct 2021)
    • Gut-Brain Axis (Jul 2021)
    • Tumor Microenvironment (Mar 2021)
    • View all review series ...
  • Viewpoint
  • Collections
    • In-Press Preview
    • Commentaries
    • Concise Communication
    • Editorials
    • Viewpoint
    • Top read articles
  • Clinical Medicine
  • JCI This Month
    • Current issue
    • Past issues

  • Current issue
  • Past issues
  • Specialties
  • Reviews
  • Review series
  • Conversations with Giants in Medicine
  • Author's Takes
  • In-Press Preview
  • Commentaries
  • Concise Communication
  • Editorials
  • Viewpoint
  • Top read articles
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Alerts
  • Advertising
  • Job board
  • Subscribe
  • Contact
Top
  • View PDF
  • Download citation information
  • Send a comment
  • Share this article
  • Terms of use
  • Standard abbreviations
  • Need help? Email the journal
  • Top
  • Abstract
  • Version history
  • Article usage
  • Citations to this article

Advertisement

Research Article Free access | 10.1172/JCI111795

Mucin degradation in human colon ecosystems. Isolation and properties of fecal strains that degrade ABH blood group antigens and oligosaccharides from mucin glycoproteins.

L C Hoskins, M Agustines, W B McKee, E T Boulding, M Kriaris, and G Niedermeyer

Find articles by Hoskins, L. in: JCI | PubMed | Google Scholar

Find articles by Agustines, M. in: JCI | PubMed | Google Scholar

Find articles by McKee, W. in: JCI | PubMed | Google Scholar

Find articles by Boulding, E. in: JCI | PubMed | Google Scholar

Find articles by Kriaris, M. in: JCI | PubMed | Google Scholar

Find articles by Niedermeyer, G. in: JCI | PubMed | Google Scholar

Published March 1, 1985 - More info

Published in Volume 75, Issue 3 on March 1, 1985
J Clin Invest. 1985;75(3):944–953. https://doi.org/10.1172/JCI111795.
© 1985 The American Society for Clinical Investigation
Published March 1, 1985 - Version history
View PDF
Abstract

We previously reported that the oligosaccharide chains of hog gastric mucin were degraded by unidentified subpopulations numbering approximately 1% of normal human fecal bacteria. Here we report on the enzyme-producing properties of five strains of mucin oligosaccharide chain-degrading bacteria isolated from feces of four healthy subjects. Four were isolated from the greatest fecal dilutions yielding mucin side chain-degrading activity in culture, and thus were the numerically dominant side chain-degrading bacteria in their respective hosts. Three were Ruminococcus strains and two were Bifidobacterium strains. Two Ruminococcus torques strains, IX-70 and VIII-239, produced blood group A- and H-degrading alpha-glycosidase activities, sialidase, and the requisite beta-glycosidases; these strains released greater than 90% of the anthrone-reacting hexoses from hog gastric mucin during growth in culture. The Bifidobacterium strains lacked A-degrading activity but were otherwise similar; these released 60-80% of the anthrone-reacting hexoses but not the A antigenic structures from hog gastric mucin. Only Ruminococcus AB strain VI-268 produced blood group B-degrading alpha-galactosidase activity, but this strain lacked beta-N-acetylhexosaminidases to complete degradation of B antigenic chains. When this strain was co-cultured with a strain that produced beta-N-acetylhexosaminidases, release of hexoses from blood group B salivary glycoprotein increased from 50 to greater than 90%, and bacterial growth was enhanced. The glycosidases required for side chain degradation were produced by these strains in the absence of mucin substrate, and a substantial fraction of each activity in stationary phase cultures was extracellular. In contrast, none of 16 other fecal Bacteroides, Escherichia coli, Streptococcus faecalis, and Bifidobacterium strains produced ABH blood group-degrading enzymes; other glycosidases produced by these strains were predominantly cell bound except for extracellular beta-N-acetylhexosaminidases produced by the five S. faecalis strains. We conclude that certain Bifidobacterium and Ruminococcus strains are numerically dominant populations degrading mucin oligosaccharides in the human colon due to their constitutive production of the requisite extracellular glycosidases including blood group antigen-specific alpha-glycosidases. These properties characterize them as a functionally distinct subpopulation of normal human enteric microflora comprised of specialized subsets that produce blood group H antigen-degrading glycosidases alone or together with either blood group A- or B-degrading glycosidases.

Browse pages

Click on an image below to see the page. View PDF of the complete article

icon of scanned page 944
page 944
icon of scanned page 945
page 945
icon of scanned page 946
page 946
icon of scanned page 947
page 947
icon of scanned page 948
page 948
icon of scanned page 949
page 949
icon of scanned page 950
page 950
icon of scanned page 951
page 951
icon of scanned page 952
page 952
icon of scanned page 953
page 953
Version history
  • Version 1 (March 1, 1985): No description

Article tools

  • View PDF
  • Download citation information
  • Send a comment
  • Share this article
  • Terms of use
  • Standard abbreviations
  • Need help? Email the journal

Metrics

  • Article usage
  • Citations to this article

Go to

  • Top
  • Abstract
  • Version history
Advertisement
Advertisement

Copyright © 2022 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

Sign up for email alerts